Folate fortification and supplementation—Are we there yet?

Bar‐Oz, Benjamin; Koren, Gideon; Nguyen, Patricia; Kapur, Bhushan

doi:10.1016/j.reprotox.2008.04.010

Cited by 38 publications

(29 citation statements)

References 70 publications

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“…This increase in blood folate compares favourably to our observed increase of 51% in mean RBC folate concentration after ingestion of 140 μg folic acid/day over 40 weeks. Furthermore, the proportion of study participants in the 140 μg/day group having a RBC folate concentration ≥906 nmol/L (65%) is also consistent with the 60–70% of reproductive age Canadian women reported to have attained this optimal level of blood folate after mandatory folate fortification of the food supply [34,35]. …”

Section: Discussionsupporting

confidence: 65%

Folate Status of Reproductive Age Women and Neural Tube Defect Risk: The Effect of Long-Term Folic Acid Supplementation at Doses of 140 µg and 400 µg per Day

et al. 2011

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Primary prevention of most folate-responsive neural tube defects (NTDs) may not require 400 μg folic acid/day but may be achieved by attaining a high maternal folate status. Using RBC folate ≥906 nmol/L as a marker for NTD risk reduction, the study aimed to determine the change in blood folate concentrations in reproductive age women in response to long-term folic acid supplementation at 400 µg/day and 140 µg/day (dose designed to mimic the average daily folic acid intake received from New Zealand’s proposed mandatory bread fortification program). Participants were randomly assigned to a daily folic acid supplement of 140 µg (n = 49), 400 µg (n = 48) or placebo (n = 47) for 40 weeks. RBC folate concentrations were measured at baseline, and after 6, 12, 29 and 40 weeks. At 40 weeks, the overall prevalence of having a RBC folate <906 nmol/L decreased to 18% and 35% in the 400 µg and 140 µg groups, respectively, while remaining relatively unchanged at 58% in the placebo group. After 40 weeks, there was no evidence of a difference in RBC folate between the two treatment groups (P = 0.340), nor was there evidence of a difference in the odds of a RBC folate <906 nmol/L (P = 0.078). In conclusion, the average daily intake of folic acid received from the proposed fortification program would increase RBC folate concentrations in reproductive age women to levels associated with a low risk of NTDs.

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Section: Discussionsupporting

confidence: 65%

Folate Status of Reproductive Age Women and Neural Tube Defect Risk: The Effect of Long-Term Folic Acid Supplementation at Doses of 140 µg and 400 µg per Day

et al. 2011

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“…9 In a 2008 Ontario review of laboratory databases, 40% of women of childbearing age were not achieving a red blood cell folate concentration of 906 nmol/L or greater. 21 Further, a recent randomized controlled trial in Toronto involving pregnant women, most of whom were consuming prenatal supplements containing folic acid (1 mg/d), showed a baseline geometric mean red blood cell folate in three groups that ranged from 2453 to 3635 nmol/L. 22 Some medical practitioners argue that many women of childbearing age need high-dose folic acid supplements and that doubling the level of folic acid fortification in the food supply should be considered.…”

Section: Discussionmentioning

confidence: 99%

Folate status of the population in the Canadian Health Measures Survey

Colapinto¹,

O’Connor²,

Tremblay³

2010

Canadian Medical Association Journal

152

133

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“…The mouse FA supplementation studies suggest that higher doses of FA than currently used may provide better protection against birth defects during human pregnancy as well, when provided at conception. Complete protection against human neural tube defects is defined as red blood cell FA concentration above 900 nmol/l [59]. However, 40% of women of child-bearing age and 36% of pregnant women exhibited RBC folate levels below 900 nmol/L[59].…”

Section: Folate and Myo-inositol Protection Of The Embryo To Prevent mentioning

confidence: 99%

Folate protection from congenital heart defects linked with canonical Wnt signaling and epigenetics

Linask

Huhta

2010

Current Opinion in Pediatrics

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Purpose of review-Environmental factors, such as drugs, chemicals, or abnormal concentrations of natural metabolites induce birth defects. Environmental effects on cardiogenesis have been little studied in contrast to neurogenesis. This review presents evidence on three environmental factors, alcohol, the drug lithium (Li), and the metabolite homocysteine (HCy), impacting the Wnt/β-catenin pathway during cardiac development and folate (FA) protection.Recent findings-Animal and epidemiological studies have shown that FA protects the embryo from birth defects. New animal studies demonstrate that FA prevents cardiovascular defects induced by Li, HCy, or alcohol, but protection occurs at a higher concentration than currently used in vitamin supplements. The data indicate that FA in combination with myo-inositol may further reduce the risk of birth defects. Discussion is presented of the cell specification stages that are impacted resulting in cardiac defects, how Wnt/β-catenin signaling is involved, and how FA and myo-inositol additively may protect embryonic pathways. The possible epigenetic role of folate in Wnt/β-catenin signaling is described.Summary-This review will enable better counseling of women by defining, during early pregnancy, a susceptible window of embryonic exposure leading to a high risk of cardiac defects, and provides a therapeutic means and the necessary timing for prevention of environmentally induced birth defects.

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Folate fortification and supplementation—Are we there yet?

Cited by 38 publications

References 70 publications

Folate Status of Reproductive Age Women and Neural Tube Defect Risk: The Effect of Long-Term Folic Acid Supplementation at Doses of 140 µg and 400 µg per Day

Folate Status of Reproductive Age Women and Neural Tube Defect Risk: The Effect of Long-Term Folic Acid Supplementation at Doses of 140 µg and 400 µg per Day

Folate status of the population in the Canadian Health Measures Survey

Folate protection from congenital heart defects linked with canonical Wnt signaling and epigenetics

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